Brain lesions incurred early in life produce a different brain from that reached after normal development. The lesion-induced modifications are specific & ordered and they contribute to sparing of cognitive processes that are severely handicapped by equivalent lesions incurred by the mature brain. The long-term goal is to identify classes of spared functions and the structures contributing to them. The specific aim of the proposed work is to test the two component hypothesis that: 1) cognitive functions are spared by early lesions of areas 17 & 18, & 2) the contributions to cognition made by middle suprasylvian (MS) cortex, in the parietal region, and by ventral posterior suprasylvian (vPS) cortex, in the temporal region, differ from contributions the same regions make to cognition & behavior in the intact brain. Normally these two regions make clearly discriminable, and non-overlapping, contributions to cognition of space & action, and to learning, memory & recognition of forms. Studies will be carried out on mature cats that incurred damage of areas 17 & 18 on P1, P28, and in adulthood (P180), and normative data will be collected from intact cats. After extensive training on a battery of behavioral tasks designed to define the magnitude of the cognitive sparing, cooling loops will be implanted to temporarily deactivate MS or vPS cortices and assess the contributions the two regions make to the spectrum of spared functions. The behavioral tasks will reveal: 1) classes of spared cognitive functions; 2) age dependent differences in sparing; 3) whether remaining MS & vPS regions adopt functions normally associated with areas 17 & 18; & 4) whether functions normally localized to either MS or vPS cortices become dispersed, as substantial rewirings suggest. The work will provide detailed information on the capacities of the immature cerebral cortex to compensate for cognitive functions severely handicapped following equivalent damage of the mature cerebrum. The identification of these capacities is important for comprehending the spectrum of consequences of early cerebral cortical damage, and for developing therapeutic strategies that attempt to enhance the sparing of cognitive functions.